Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040586 (tracheobronchitis)
 449 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aspergillus is a ubiquitous dimorphic fungus that causes a variety of human diseases ranging in severity from trivial to life-threatening, depending on the host response. An intact host defence is important to prevent disease, but individuals with pre-existing structural lung disease, atopy, occupational exposure or impaired immunity are susceptible. Three distinctive patterns of aspergillus-related lung disease are recognized: saprophytic infestation of airways, cavities and necrotic tissue; allergic disease including extrinsic allergic alveolitis, asthma, allergic bronchopulmonary aspergillosis, bronchocentric granulomatosis and chronic eosinophilic pneumonia; and airway and tissue invasive disease -- pseudomembranous tracheobronchitis, acute bronchopneumonia, angioinvasive aspergillosis, chronic necrotizing aspergillosis and invasive pleural disease. A broad knowledge of these clinical presentations and a high index of suspicion are required to ensure timely diagnosis and treatment of the potentially lethal manifestations of aspergillus-related pulmonary disease. In the present report, the clinical, radiographic and pathological aspects of the various aspergillus-related lung diseases are briefly reviewed.
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PMID:Aspergillus-related lung disease. 1630 29

Mycoplasmas cause chronic inflammation and are implicated in asthma. Mast cells defend against mycoplasma infection and worsen allergic inflammation, which is mediated partly by histamine. To address the hypothesis that mycoplasma provokes histamine release, we exposed mice to Mycoplasma pulmonis, comparing responses in wild-type and mast cell-deficient KitW-sh/KitW-sh (W-sh) mice. Low histamine levels in uninfected W-sh mice confirmed the conventional wisdom that mast cells are principal sources of airway and serum histamine. Although mycoplasma did not release histamine acutely in wild-type airways, levels rose up to 50-fold above baseline 1 week after infection in mice heavily burdened with neutrophils. Surprisingly, histamine levels also rose profoundly in infected W-sh lungs, increasing in parallel with neutrophils and declining with neutrophil depletion. Furthermore, neutrophils from infected airway were highly enriched in histamine compared with naive neutrophils. In vitro, mycoplasma directly stimulated histamine production by naive neutrophils and strongly upregulated mRNA encoding histidine decarboxylase, the rate-limiting enzyme in histamine synthesis. In vivo, treatment with antihistamines pyrilamine or cimetidine decreased lung weight and severity of pneumonia and tracheobronchitis in infected W-sh mice. These findings suggest that neutrophils, provoked by mycoplasma, greatly expand their capacity to synthesize histamine, thereby contributing to lung and airway inflammation.
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PMID:Neutrophil histamine contributes to inflammation in mycoplasma pneumonia. 1715 62

Systemic colistin has shown efficacy against multidrug-resistant Pseudomonas aeruginosa and Acinetobacter spp., but it has presented poor results in pneumonia. Aerosolized polymyxin in cystic fibrosis patients has had good results. In this study, inhaled polymyxin B was used to treat respiratory infections by multidrug-resistant Gram-negative bacilli (MR-GNBs). Nineteen patients were treated with inhaled polymyxin B: 14 pneumonia, most of which had previously failed treatment with intravenous polymyxin B, and 5 tracheobronchitis. Inhaled polymyxin B was given at the dose of 500,000 IU twice a day after an aerosolized beta(2)-agonist. In pneumonia, inhaled and intravenous polymyxin B was given together. Median age was 69 years; 89% were in the intensive care unit. Sixteen infections (84%) were caused by P. aeruginosa. Klebsiella pneumoniae, Alcaligenes xylosoxidans, and Burkholderia sp. caused one infection each. In the 14 pneumonia cases, median of previous use of intravenous polymyxin B was 20 days (range, 0-32). Inhaled polymyxin B was used for a mean of 14 days (range, 4-25). Cure occurred in 10 (53%) patients, improvement in 8 (42%), and failure in 1. Nine patients died during hospitalization (all with pneumonia). Adverse events occurred in 4 patients without interruption of inhalation. This is the largest report using inhaled polymyxin B to treat nosocomial pneumonia by MR-GNB that had failed intravenous polymyxin B. It was also effective alone in P. aeruginosa tracheobronchitis.
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PMID:Salvage treatment of pneumonia and initial treatment of tracheobronchitis caused by multidrug-resistant Gram-negative bacilli with inhaled polymyxin B. 1735 Feb 1

Ventilator-associated pneumonia (VAP) significantly increases intensive care unit morbidity, mortality, and costs. VAP is thought to be caused by bacterial entry into injured airways, which produces tracheobronchitis that evolves into diffuse pneumonia. The use of aerosolized antibiotics is conceptually attractive, especially when the infection is early and limited to the airway epithelium. Data show that aerosolized antibiotics kill airway bacteria and improve outcomes in cystic fibrosis. The clinical evidence for aerosolized antibiotics to prevent VAP is weak but suggestive. Concerns about the high cost, possible development of antibiotic resistance, and other potential risks of aerosolized antibiotics led several evidence-based consensus groups to recommend against routine use of aerosolized antibiotics for VAP prevention until better data are available. Importantly, the clinical evidence that aerosolized antibiotics can treat established VAP is negative, and multiple consensus groups recommend against treating established VAP with aerosolized antibiotics.
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PMID:Respiratory therapies in the critical care setting. Should aerosolized antibiotics be administered to prevent or treat ventilator-associated pneumonia in patients who do not have cystic fibrosis? 1741 76

Enterobacter cloacae has been associated with several outbreaks, usually involving strains that overproduce chromosomal beta-lactamase or, uncommonly, strains expressing extended-spectrum beta-lactamases (ESBL). Only sporadic cases of ESBL-producing E. cloacae have been identified in our hospital in recent years. We describe the epidemiology and clinical and microbiological characteristics of an outbreak caused by ESBL-producing E. cloacae in a cardiothoracic intensive care unit (CT-ICU). Prospective surveillance of patients with infection or colonization by ESBL-producing E. cloacae among patients admitted to the CT-ICU was performed during the outbreak. Production of ESBL was determined by decreased susceptibility to expanded-spectrum cephalosporins and a positive double-disk test result. Clone relatedness was determined by pulsed-field gel electrophoresis (PFGE). From July to September 2005, seven patients in the CT-ICU with ESBL-producing E. cloacae were identified (four males; median age, 73 years; range, 45 to 76 years); six patients had cardiac surgery. Four patients developed infections; three had primary bacteremia, one had ventilator-associated pneumonia, and one had tracheobronchitis. ESBL-producing E. cloacae showed resistance to quinolones and aminoglycosides. PFGE revealed two patterns. Five isolates belonged to clone A; two carried a single ESBL (pI 8.2 and a positive PCR result for the SHV type), and three carried two ESBLs (pIs 8.1 and 8.2 and positive PCR results for the SHV and CTX-M-9 types). Isolates belonging to clone B carried a single ESBL (pI 5.4 and a positive PCR result for the TEM type). Review of antibiotic consumption showed increased use of cefepime and quinolones during June and July 2005. The outbreak was stopped by the implementation of barrier measures and cephalosporin restriction. ESBL production could be increasingly common in nosocomial pathogens other than Escherichia coli or Klebsiella pneumoniae.
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PMID:Nosocomial outbreak due to extended-spectrum-beta-lactamase- producing Enterobacter cloacae in a cardiothoracic intensive care unit. 1758 32

Two large intensive care centers performed a prospective controlled, randomized study evaluating the efficiency of closed aspiration systems in the prevention of lower respiratory tract infections during sustained artificial ventilation. Analysis of the results of the study has ascertained that the closed aspiration systems make it possible to attenuate a colonization process and further lower respiratory tract infection, by statistically significantly reducing the risk of tracheobronchitis and pneumonia.
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PMID:[Role of closed aspiration systems in the prevention of lower respiratory tract infections during artificial ventilation]. 1768 84

Data on postmortem examination of five patients deceased during Legionnaires' outbreak in town Verkhnyaya Pyshma are presented in the article. Feature of course of the disease was severe affection of the lungs with development of toxic shock. Pathomorphological picture in lungs was characterized by polymorphism, presence of shock reaction and ventilator-associated pneumonia (atelectases, distelectases, tracheobronchitis). In autopsy material from four fatal cases Legionella pneumophila serogroup 1 was detected. Causative agent of pneumonia was not determined in one fatal case although comparison of clinical and morphological characteristics of this case with other four cases as well as detection of Gram-negative bacillus in alveolar macrophages allowed to consider this case of pneumonia as caused by Legionella. In studied fatal cases postmortem diagnoses were ascertained in which main disease was bilateral pneumonia caused by Legionella pneumophila serogroup 1 complicated by toxic shock.
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PMID:[Pathologic anatomy of pneumonia caused by Legionella: on the materials of outbreak in town Verkhnyaya Pyshma]. 1846 92

Nosocomial lower respiratory tract infections are a common cause of morbidity and mortality in intensive care unit (ICU) patients. Although many studies have investigated the management and prevention of ventilator-associated pneumonia (VAP), few have focused on ventilator-associated tracheobronchitis (VAT). In this issue of Critical Care, Nseir and coworkers present interesting data from a randomized controlled study of antimicrobial therapy for VAT. Patients randomly assigned to antibiotic therapy had more mechanical ventilation-free days (P < 0.001), fewer episodes of VAP (13% versus 47%; P < 0.001), and a lower ICU mortality rate (18% versus 47%; P = 0.05) than those without antibiotic therapy. Although this study has limitations, the data suggest that VAT may be an important risk factor for VAP or overlap with early VAP. More importantly, targeted antibiotic therapy for VAT may improve patient outcomes and become a new paradigm for prevention or early therapy for VAP.
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PMID:Ventilator-associated tracheobronchitis (VAT): questions, answers, and a new paradigm? 1845 64

Genetic reassortment of H5N1 highly pathogenic avian influenza viruses (HPAI) with currently circulating human influenza A strains is one possibility that could lead to efficient human-to-human transmissibility. Domestic pigs which are susceptible to infection with both human and avian influenza A viruses are one of the natural hosts where such reassortment events could occur. Virological, histological and serological features of H5N1 virus infection in pigs were characterized in this study. Two- to three-week-old domestic piglets were intranasally inoculated with 10(6) EID(50) of A/Vietnam/1203/04 (VN/04), A/chicken/Indonesia/7/03 (Ck/Indo/03), A/Whooper swan/Mongolia/244/05 (WS/Mong/05), and A/Muscovy duck/Vietnam/ 209/05 (MDk/VN/05) viruses. Swine H3N2 and H1N1 viruses were studied as a positive control for swine influenza virus infection. The pathogenicity of the H5N1 HPAI viruses was also characterized in mouse and ferret animal models. Intranasal inoculation of pigs with H5N1 viruses or consumption of infected chicken meat did not result in severe disease. Mild weight loss was seen in pigs inoculated with WS/Mong/05, Ck/Indo/03 H5N1 and H1N1 swine influenza viruses. WS/Mong/05, Ck/Indo/03 and VN/04 viruses were detected in nasal swabs of inoculated pigs mainly on days 1 and 3. Titers of H5N1 viruses in nasal swabs were remarkably lower compared with those of swine influenza viruses. Replication of all four H5N1 viruses in pigs was restricted to the respiratory tract, mainly to the lungs. Titers of H5N1 viruses in the lungs were lower than those of swine viruses. WS/Mong/05 virus was isolated from trachea and tonsils, and MDk/VN/05 virus was isolated from nasal turbinate of infected pigs. Histological examination revealed mild to moderate bronchiolitis and multifocal alveolitis in the lungs of pigs infected with H5N1 viruses, while infection with swine influenza viruses resulted in severe tracheobronchitis and bronchointerstitial pneumonia. Pigs had low susceptibility to infection with H5N1 HPAI viruses. Inoculation of pigs with H5N1 viruses resulted in asymptomatic to mild symptomatic infection restricted to the respiratory tract and tonsils in contrast to mouse and ferrets animal models, where some of the viruses studied were highly pathogenic and replicated systemically.
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PMID:Domestic pigs have low susceptibility to H5N1 highly pathogenic avian influenza viruses. 1861 94

Nosocomial lower respiratory tract infections are a common cause of morbidity and mortality in ICU patients receiving mechanical ventilation. Many studies have investigated the management and prevention of ventilator-associated pneumonia (VAP), but few have focused on the role of ventilator-associated tracheobronchitis (VAT). The pathogenesis of lower respiratory tract infections often begins with tracheal colonization that may progress to VAT, and in selected patients to VAP. Since there is no well-established definition of VAT, discrimination between VAT and VAP can be challenging. VAT is a localized disease with clinical signs (fever, leukocytosis, and purulent sputum), microbiologic information (Gram stain with bacteria and leukocytes, with either a positive semiquantitative or a quantitative sputum culture), and the absence of a new infiltrate on chest radiograph. Monitoring endotracheal aspirates has been used to identify and quantify pathogens colonizing the lower airway, to diagnose VAT or VAP, and to initiate early, targeted antibiotic therapy. Recent data suggest that VAT appears to be an important risk factor for VAP and that targeted antibiotic therapy for VAT may be a new paradigm for VAP prevention and better patient outcomes.
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PMID:Ventilator-associated tracheobronchitis: the impact of targeted antibiotic therapy on patient outcomes. 1980 81


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